Neutrophil attractant protein

Yoshimura T, Johnson DG. cDNA cloning and expression of guinea pig neutrophil attractant protein-1 (NAP-1) NAP-1 is highly conserved in guinea pig. J Immunol 1993 151 6225-6236. 

Sylvester I, Yoshimura T, Sticherling M, et al. Neutrophil attractant protein-1-immunoglobulin G immune complexes and free anti-NAP-1 antibody in normal human serum. J Clin Invest 1992 90 471-481. 

Rot, A. (1993). Neutrophil attractant/activation protein-1 (interleukin-8) induces in vitro neutrophil migration by haptotactic mechanism. Eur. J. Immunol. 23, 303-306. 

Leonard, E., Skeel, A., Yoshimura, T., Noer, K., Kutvirt, S., and Van Epps, D., Leukocyte specificity and binding of human neutrophil attractant/activation protein-1, J. Immunol., 144, 1323, 1990. 

Beall, C. J., Mahajan, S., and Kolattukudy, P. E. (1992). Conversion of monocyte chemoattractant protein-1 into a neutrophil attractant by substitution of two amino acids. J. Biol. Chem. 267, 2455-2459. 

Wuyts A, Proost P, Lenaerts JP, Ben-Baruch A, Van Damme J, Wang JM Differential usage of the CXC chemokine receptors 1 and 2 by interleukin-8, granulocyte chemotactic protein-2 and epithelial-cell-derived neutrophil attractant-78. Eur J Biochem 1998 255 67. 

Sylvester, I., Rankin, J. A., Yoshimura, T., Tanaka, S., and Leonard, E. J. (1990) Secretion of neutrophil attractant/activation protein (NAP-1) by lipopolysaccharide-stimulated lung macrophages determined by both enzyme-linked immunosorbent assay and N-terminal sequence analysis. Am. Rev. Respir. Dis. 141, 683-688. 

Pulmonary granuloma formation induced by infusion of 5 mg particulate glucan/rat was markedly reduced when neutrophils were depleted by rabbit antiserum directed against rat peripheral blood neutrophils or by catalase (15,000 U/raf) at the time of injection and 24 h after glucan infusion (Kilgore et al. 1997). Neutrophils and reactive oxygen intermediates (H2O2) are required for the local induction of monocyte attractant protein-1 to be secreted by endothelial cells. 

Exposure of the SECs to pathogens or cytokines produced by other cells during stress induces activation of the SECs and subsequent production of cytokines, eicosanoids, and/or adhesion molecules. For instance, after activation with EPS, a main component of the walls of gramnegative bacteria and a major inducer of inflammation and non-specific immune functions [20], SECs produce a number of pro- and anti-inflammatory cytokines. Pro-inflammatory cytokines shown to be produced were tumour necrosis factor alpha (TNFa) [26] interleukin-1 alpha/beta(IL-lo/p) [27] the major inducer of acute phase proteins interleukin-6 (IL-6) [28] and the neutrophil chemo-attractant interleukin-8 (IL-8) [29]. Anti-inflammatory cytokines shown to be produced were interleukin-10 (IL-10) [27] and hepatocyte growth factor (HGF) [30]. 

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. 

---